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Background: To get more insight into the effects of the most widely used antiepileptic drugs (AEDs) on the pro oxidant/ antioxidant balance in epilepsy, a comparative analysis of the byproducts of oxidative damage and antioxidant defense mechanisms was performed in patients with epilepsy treated with lamotrigine, carbamazepine and valproic acid. Methods: Byproducts of oxidative damage to proteins (reactive carbonyl derivatives, RCD and protein thiol groups, PSH), lipids (urinary isoprostanes, 8-epi-PGF2a) and DNA (urinary 8-hydroxy-2’-deoxyguanosine, 8-OHdG), as well as the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) were measured in 60 patients with newly diagnosed seizure (at illness onset and after 6 months of treatment with lamotrigine, carbamazepine or valproic acid) and in 20 healthy controls. Results: In patients with epilepsy, RCD, urinary 8-epi-PGF2a and 8-OHdG, together with SOD and GPX activities were significantly increased, while P-SH were only slightly decreased. After 6 months of treatment with AEDs, a decrease was observed in RCD, urinary 8-epi-PGF2a and 8- OHdG to values slightly higher or similar to the control, while P-SH remained unchanged. A decrease was also observed in SOD and GPX activities, although they remained significantly increased compared to controls. Conclusions: The results of this study have shown that treatments with lamotrigine, carbamazepine and valproic acid affect the prooxidant/antioxidant balance in patients with epilepsy.

Introduction. A sudden withdrawal of antiepileptic drugs gives higher rate of epileptic seizures in the settings of video electroencephalography (vEEG), monitoring that is a subject to further registration and analysis. A very rare complication of this method is transient lesion of the splenium of corpus callosum (SCC) detected with brain MRI. Case report. We presented a patient with a 5-year history of pharmacoresistant epilepsy admitted to the Institute of Neurology (August, 2008) for vEEG monitoring. Interictal epileptic discharges but none seizure were recorded after the sudden withdrawal of antiepileptic medications, during 5 days of vEEG monitoring Initial brain MRI three days after vEEG monitoring revealed focal lesion in SCC, hyperintense on T2 and FLAIR sequence. A longitudinal radiological follow-up (7 and 49 days after initial acquisition) confirmed transient nature of the lesion without diffusion coefficient changes. Conclusion. SCC lesion, reversible and harmless, may occur after a sudden antiepileptic withdrawal. Its early detection makes further extensive neuroradiological and clinical examinations unnecessary.

The perplexing and tantalizing disease of rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by peculiar, potentially dangerous behavior during REM sleep. It was described both in animals and humans. RBD in mammals was first described by Jouvet and Delorme in 1965, based on an experimental model induced by lesion in pontine region of cats [1]. In 1972, Passouant et al. described sleep with eye movements and persistent tonic muscle activity induced by tricyclic antidepressant medication [2], and Tachibana et al., in 1975, the preservation of muscle tone during REM sleep in the acute psychosis induced by alcohol and meprobamate abuse [3]. However, the first formal description of RBD in humans as new parasomnia was made by Schenck et al in 1986 [4-7]. Subsequently, in 1990, the International Classification of Sleep Disorders definitely recognized RBD as new parasomnia [8]. To our knowledge, arts and literature do not mention RBD. Except for the quotation, made by Schenck et al [6] in 2002, of Don Quixote de la Mancha whose behavior in sleep strongly suggested that Miguel de Servantes actually described RBD, no other artistic work has portrayed this disorder. Only recently we become aware of the cinematic presentation of RBD which by decades precedes the first scientific description. The first presentation of RBD on film was made prior to the era of advanced electroencephalography and polysomnography, and even before the discovery of REM sleep by Aserinsky and Kleitman in 1953. [9]. The artistic and intuitive presentation of RBD was produced in Technicolor in a famous film "Cinderella" created by Walt Disney in 1950, some 35 years prior to its original publication in the journal "Sleep" [2]. Since there is an earlier version of the film initially produced in 1920, presumably containing this similar scene, we can only speculate that the first cinematic presentation of RBD might precede its scientific debut by 65 years. In a scene in a barn, clumsy and goofy dog Bruno is, as dogs usually do, lying on a mat deeply asleep and obviously dreaming of his enemy cat Lucifer. This is clearly implied by a preceding scene showing Lucifer being extremely frightened while observing the dreaming dog in action. The cat Lucifer is instantly aware that the dog is chasing him in a dream and is horrified (Pictures 1-3). In a film sequence lasting only 16 seconds, we see Cinderella being aware that Bruno is firmly asleep, apparently having a terrible dream. While lying on the ground with total absence of any muscle atonia, the dog Bruno chases the cat Lucifer in his dream. He is running and barking, and when in his dream he catches Lucifer, he tries to devour the cat. Cinderella tries to wake him up by calling his name twice, first gently and then more vigorously, as she becomes aware of the content of Lucifer’s dream and his intention. The dog is deeply asleep and does not awake in spite of being exposed to sunlight through the opening door of the barn, and called by name by Cinderella (Pictures 4-14). For such a behavior he is reprimanded by Cinderella who definitely recognized the content of his dream (Pictures 15-36). Immediately upon awakening, Bruno shows his good natured temper and amiable character (Pictures 37-40). The film shows that the producer (Walt Disney) and film directors (Wilfred Jackson, Clyde Geronimi and Hamilton Luske) were obviously aware that a dog might enact the content of a dream. It also implies that their observation from day-to-day (better to say night-to-night) life of the dream enactment is not a rare phenomenon, and that it deserves to be shown in the film. These authors were also aware that dogs having RBD were good-natured during wakefulness and that only in dreams they showed unrestrained aggression; while awake, dog Bruno was only an opponent or enemy to the cat Lucifer, but in dreams the animosity grew to aggression. Disney noticed this peculiar kind of sleep behavior and most probably was aware of its frequency and importance, and certainly not knowing it is a disease, he used it to color his cartoon character making it more likable to the observer. Since the film was nominated for Best Score, Best Song and Best Sound, it not only reflected the artistic and observational abilities of the producer, but also his sense of the importance of the phenomenon, awareness of its frequency and presence in animals. The onlooker is tempted to speculate that Disney, while obviously having been aware of such a behavior in animals, might also have knowledge of its presence in humans. Even more, since Disney’s films frequently present different sleep disturbances (e.g., obstructive sleep apnea (OSA) in dwarfs, hypersomnolence in the dwarf Sleepy, or jactatio capitis nocturna in the dwarf Dopey in film "The Snow White"), it seems plausible that he first observed RBD in man, and then artistically transferred it to his cartoon animal characters. Since the whole incident took place during the day, we assume that Bruno, apart from suffering from RBD, had another sleep disorder causing daytime REM intrusions (possibly narcolepsy and probably not OSA, as is frequent in Disney’s films, since there is no excessive daytime sleepiness). The odd thing about RBD is that it may easily, as it probably did for centuries, go as peculiar behavior in sleep – rather than disease. While Lucifer was presented as sober and prudent cat, Bruno was clumsy and forgetful dog. We will refrain from speculating that dog’s clumsy nature could be the consequence of the CNS involvement by neuro-degenerative disease (i.e., synucleinopathy). Although we are aware that, in interpreting this episode we assumed to be at least as imaginative as the cartoon films of Walt Disney are, the fact remains that the artistic film presentation of RBD precedes its scientific description by at least 35 years.

The results of clinical and genetic analysis of three Serbian families (pedigrees) with autosomal dominant inheritance, incomplete penetrance and phenotypic features of GEFS+ are presented in this study. Mutation analysis of the SCN1A, SCN1B and GABRG2 genes was performed in all affected and some unaffected members of these three families. Twentysix exons of SCN1A, five exons of SCN1B and nine exons of GABRG2 were individually amplified using primers based on intronic sequence. PCR products were sequenced in both forward and reverse directions. Subsequently, the samples were run and analyzed using 377 DNA automated sequencer. No consanguinity was noticed. The MM and OM family members live in Republic of Srpska while KS family originates from the central Serbia. No mutations of the exons of SCN1A, SCN1B and GABRG2 genes were found in tested subjects. Obligate carriers in MM family (III-1, III-2, and III-4) exhibit variable expressivity or incomplete penetrance rather than proof of polygenetic inheritance. OM pedigree follows autosomal dominant pattern despite reduced penetrance. Bilinear transmission may assume the possibility of multigenetic mode of inheritance in KS family. The fact that all affected members in three Serbian families were negative for mutations in SCN1A, SCN1B and GABRG2 genes strongly supports the hypothesis of significant genetic heterogeneity of GEFS+. Recognizing GEFS+ on clinical grounds contributes to more precise integration of this syndrome into already existing classification of epileptic syndromes.

INTRODUCTION Psychogenic nonepileptic seizure (PNES) is a sudden change in a person's behavior, perception, thinking, or feeling that is usually time limited and resembles, or is mistaken for, epilepsy but does not have the characteristic electroencephalographic (EEG) changes that accompanies a true epileptic seizure [1]. It is considered that PNES is a somatic manifestation of mental distress, in response to a psychological conflict or other Stressors [2]. A wide spectrum of clinical presentation includes syncope, generalized tonic-clonic seizure, simple and complex partial seizure, myoclonic seizure, frontal lobe seizures and status epilepticus [3]. Coexistence of epilepsy and PNES is seen in approximately 9% of cases [5]. Between 25-30% of patients referred to tertiary centers and initially diagnosed as refractory epilepsy were on further examination diagnosed as PNES [6,7]. In DSM-IV [12] PNES are usually categorized under conversion disorder with seizures or convulsions. However, psychiatric basis of PNES may be anxiousness (panic attack), somatization or factitious disorder, simulation, dissociative disorders and psychosis [1]. AIM The aim of the study was to establish clinical phenomenology and EEG characteristics as well as basic psychiatric disorder in patients with PNES. METHOD In a retrospective study covering the period from January 1st 1999 till April 31 st 2003, 24 patients (22 female, 2 male) treated at the Institute of Neurology in Belgrade were analyzed. PNES were defined as sudden change in behavior incoherent with epileptiform activity registered on EEG. Possible PNES were determined on the basis of history data and clinical examination during the attack but definitive confirmation was established only by the finding of no ictal EEG changes during typical seizure of each patient. Patients with coexisting epilepsy were included in the study, too. At least two standard EEG (range 2-6, median 4) were performed at the beginning of diagnostic evaluation. Demographic data, clinical presentation (apparent loss of consciousness, type of convulsion and associated clinical signs) and placebo-induced seizures (administration of saline near the cubital vein) with EEG or video-EEG monitoring were analyzed. Basic psychiatric disorder was classified according to DSM IV classification criteria. RESULTS Duration of PNES was 4.7 years (range from 2 months to 30 years). The time from onset to the diagnosis of PNES was 4.5 years. Epilepsy comorbidity was diagnosed in 9 patients (37.5%). The average time of use of antiepileptic drugs (AED) in the group of isolated PNES was 2.4 years and 20% of patients were treated with two or more AED. The vast majority of patients presented with bilateral convulsions (54.16%) with apparent loss of consciousness found in 91.6% of cases. Ictal iwury (16.7%), tongue bite (4.2%) and premonition of the seizure (17.4%) were uncommon. Variability in clinical presentation of seizures was found in over half of patients (57%). Psychological trigger could be determined in over 60% of patients. EEG findings in a group with isolated PNES suggesting the existence of epileptiform activity was found in one case. EEG monitoring of placebo-induced seizure was performed in 20 patients, of whom 19 (95%) showed typical habitual attack with no electroclinical correlate. In 70% of cases conversion disorder DSM-IV criteria were fulfilled. Somatization disorder and undifferentiated somatoform disorder were found in 3 patients. The diagnosis of factitious disorder was made in one case and only two patients were undiagnosed according to DSM-IV. DISCUSSION Average delay from onset to diagnosis of PNES in larger studies was estimated to be approximately 7 years [8]. Even though diagnostic delay in our study was shorter, organizational reasons for this could not be found. Longer duration of a typical attack (compared to the epileptic seizure), apparent loss of consciousness, bilateral convulsion behavior and significant clinical variability in absence of typical epileptic elements such as tongue bite and ictal iwury could be the main clinical manifestation of PNES. We found rare interictal abnormalities (6.7%) in the group with isolated PNES and significant percentage (77.7%) in patients with coexisting epilepsy which is coherent with other reports [8]. The latest could lead to prolonged delay in appropriate diagnosis and suitable treatment. Clear psychological trigger wasn't noted in whole group of patients (61 %). This, however, is not unusual since PNES represents a chronic disorder with repeated triggering that could lead to less significant role of the same psychological trigger in developed PNES. Even insufficiently resolved in ethical terms, placebo-induced procedure was of huge sensitivity. In clinical practice conversion disorder is hard to differ from malingering or implementation of secondary gain. One could make the conclusion only on the basis of detailed and careful estimation of the symptoms developing context Conversion disorder is more prevalent among women (from 2:1 to 10:1) [4, 13] but modest percentage of affected men could be explained only by limited sample in this study. CONCLUSION PNES is often replaced with epilepsy and in number of cases clinical differentiation is not easy. One should be acquainted with clinical presentation of PNES as well as its psychiatric origin in order to adequately recognize and treat the disorder.

In patients with partial seizures controlled-release vs. conventional carbamazepine had better efficiency, based on an excellent tolerance favorable daily dosage and superior compliance.

Concussive convulsions are motor manifestations in acute head injury. This clinical phenomenon should be distin- guished from epileptic seizures. We present two young men with motor and convulsive manifestations in acute head injury. Patient 1. A18-year old basketball player felt on the parquet during a game. Initially he was struck on the right shoulder which caused brief and vigorous twitch of the head towards the ground and additional temporal impact. At the moment of impact he lost consciousness and developed tonic leg and arm posturing with both clenched fists. His legs were extended during next 20 seconds. Thereafter he was still and his loss of consciousness lasted 3 minutes. Patient 2. A 26-year old man felt on the wooden ground from a 4 m high ferry. He got head impact and lost consciousness. In a few seconds he had tonic/clonic convulsions for the next 10-15 seconds. Ten minutes later he awaked. Results of subsequent neurological examination, electroencephalography and cerebral magnetic resonance imaging studies were normal in both patients. They returned to their occupations after four weeks without problems for a further one year. Conclusion. Described motor manifestations present concussive convulsions. These clinical features are due to transient functional decerebration and corticomedullary dissociation during cerebral concussion. Concussive convulsions are a non-epileptic phenomenon, they are not associated with structural brain injury and have good prognosis. Antiepileptic treatment is not indicated.

Introduction. It is considered that around 20%-30% of patients of all ages and in all continents have wrong epilepsy diagnoses. Diagnostic and consequential therapeutic errors appear, most often, when an adequate diagnostics is not applied. Benign focal epilepsy of childhoods with centrotemporal spikes-rolandic epilepsy, brings very often to diagnostic and therapeutic problems because of persistence of epilepticforms changes in an electroencephalography (EEG) recording, several years after establishment of good control over seizures. Case report. We presented 8.5 years-old girl, with the first and the only epileptic seizure at the age of 5, during her sleep. With a clear correlation of EEG record, benign rolandic epilepsy was diagnosed, so the therapy with valproate was introduced. There were no seizures after three years of its implementation. Because of epileptic-forms changes that still persisted in EEG record during her sleep, it was suggested to further use valproate. However, after reconsidering all circumstances it was concluded that the AED should bee slowly reduced up to its exclusion. After a complete stoppage of the therapy, the patient did not have any epileptic seizure for nine months, although EEG still remained pathologically changed during her sleep. Conclusion. A changed EEG record in a patient with rolandic epilepsy must not be a predictor of continuation of antiepileptic drugs therapy, after 2-3 years of successful seizures remission.

The association of arachnoiditis ossificans with acquired peripheral nerve disease is rare. We report a case who presented with progressive myelopathy due to arachnoiditis ossificans from prior trauma, complicated with multifocal motor neuropathy. Intradural bone was removed at surgery. [ABSTRACT FROM AUTHOR]